Healthspan and lifespan diverge biologically: living a long life does not automatically mean ageing in good health. Research into approaches that specifically extend the healthy phase of life is moving rapidly but remains largely in the stage of animal models and small human studies. Dietary restriction and fasting have the strongest evidence base in humans; widely discussed compounds such as NMN have so far been studied too little for firm conclusions.
Lifespan and healthspan measure two different things. Lifespan is simply how long a person lives, measured in years. Healthspan is how long a person lives in good health, meaning without serious chronic disease and with good physical and cognitive functioning. In practice, the two do not go hand in hand at all: reaching old age does not automatically mean ageing healthily. Ageing researchers are drawing this distinction ever more explicitly, and new interventions therefore focus primarily on extending the healthy period of life rather than merely adding years.
The divergence between the two concepts is already apparent from the way biological ageing is measured. An epigenetic biomarker that measures how quickly the body ages biologically, independent of calendar age, predicts risk of death, cancer, reduced physical functioning and Alzheimer's disease better than calendar age alone. In other words, two people of the same age can differ substantially in biological terms, and that difference translates into health outcomes, not just survival.
Cellular ageing is one of the mechanisms behind this divergence. As people grow older, so-called senescent cells accumulate: cells that no longer divide but continuously secrete pro-inflammatory substances. This leads to chronic low-grade inflammation and tissue damage, impairing health without necessarily shortening life by much. A comparable mechanism operates in autophagy, the cellular cleaning process by which damaged proteins are broken down: this process weakens with age, contributing to loss of function without directly shortening lifespan.
Dietary restriction combined with adequate nutrition is, to date, the best-supported approach for extending both healthspan and lifespan. This has been demonstrated in multiple animal species, including rodents and primates. In humans there are indications of comparable physiological effects, but direct evidence that it also extends human life is still lacking. Fasting over shorter periods (12 to 48 hours repeatedly, or 2 to 7 days per month) shows positive effects in human studies on risk factors for cancer, cardiovascular disease, neurodegeneration and metabolic disease, and works partly through the stimulation of autophagy. Side effects with longer fasting periods are possible and deserve attention.
Promising indications also come from gut microbiome research and from studies with senolytics. In mouse models of accelerated ageing, a microbiome transplant from healthy mice substantially improved health and lifespan, even when only the bacterium Akkermansia muciniphila was administered. Drugs that clear senescent cells or inhibit their harmful secretions extend the healthy phase of life in animal models. Both approaches are, however, still at an early stage of research in humans. Finally, NMN supplementation (300 to 900 mg per day) has been tested in a small RCT of 80 participants over 60 days: physical performance and self-reported health improved, but this is a short-term, small study with partial industry funding, and whether it delivers real long-term healthspan gains remains unknown.
Claims are based on multiple publications (PMID 29676998, 31292558, 34518687, 35310455, 31332389, 35015337, 34563704, 36482258). Most findings on mechanisms and interventions come from animal models or small human studies. Dietary restriction has the broadest evidence base. NMN data are limited in duration and sample size, with commercial interests involved. No large randomised trials on real long-term healthspan in humans are available.